Vernal conjunctivitis (VC), a bilateral conjunctival disease, is a cause of significant eye disease in many individuals each year. The seasonal incidence, the presence of eosinophils in conjunctival secretions and the response to topical or systemic steroid therapy suggest an immune hypersensitivity reaction to an environmental agent. The proposed study is designed to elucidate the pathogenesis of tissue injury and the etiology of this disease. External ocular secretions (tear fluid) of VC patients with negative immediate intradermal skin reactivity will be examined for components or mediators of an immune-mediated hypersensitivity process. The presence of specific antibodies to environmental allergens (mold and pollen antigens) will be studied in tear fluid by the radioallergosorbent test (RAST) for specific IgE antibodies and by radioimmunodiffusion for specific IgA, IgM and IgG antibodies. The detection of specific antibodies in tears would identify the environmental factor(s) important in the etiology of this disease. Tear fluids will be examined for the presence of immune complexes and complement components which might suggest a complement-mediated hypersensitivity mechanism. Direct evidence for an immune mechanism in the pathogenesis of VC will be sought by examining tear fluids for biologically active mediators of inflammation. Since eosinophils in the conjunctival secretions are a prominent feature of VC, tear secretions will be studied for the presence of a factor(s) which influences the migration of eosinophils. An IgE-mediated, a complement-derived or T-cell mediated immune mechanism can result in the generation of an eosinophilic chemotactic factor (ECF). The characterization and identification of this ECF in tears plus the other studies outlined above would define the immune hypersensitivity mechanism(s) which plays an important role in the pathogenesis of VC.